Addiction vulnerability genes include those that are likely to harbor allelic variants that contribute to human individual differences in vulnerability to addictions. During this and prior years, we identified dozens of candidates to play such roles based on the covergences between nominally-positive data derived from up to fourteen separate abuser/control or quit success comparisons. During the current year we have reported iincreasing support from outside samples/datasets for the genes that we have identified most consistently in our own data. We added to evidence supporting roles for many of these genes with additional data from several comparisons between nicotine depdendent and control samples and substance dependent and control samples with higher marker densities. We added additional support from comparisons between smokers who were successful vs unsuccessful in quitting in clinical trials and in community samples. We added novel data concerning rate of uptake of developmental use of addictive substances. Genes identified in this fashion include a disproportionate number of genes whose products are involved in cell adhesion molecule actions. During this year we identified additional functional variation at a locus that contain these genes, focusing on an extended haplotype that alters level of expression for CDH13. These data provide the basis for animal models that replicate, at least in part, findings in humans. During this year, we reported association between a specific addiction vulnerability phenotype, preference for mentholated cigarettes, and haplotypes in the TRPA1 channel that serves as a menthol receptor. During the year, we identified associations between these TRPA1 haplotypes and levels of TRPA1 expression in allelc specific expression studies of mRNAs extracted from postmortem human dorsal medullas.